Oncotarget

http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=19269&path[]=61662

Volume 11, Issue 28 of Oncotarget features "Lipid and protein tumor markers for head and neck squamous cell carcinoma identified by imaging mass spectrometry" by Schmidt et, al. which reported that the authors used MALDI imaging mass spectrometry and immunohistochemistry to seek tumor-specific expression of proteins and lipids in HNSCC samples.

DOI - https://doi.org/10.18632/oncotarget.27649

Full text - https://www.oncotarget.com/article/27649/text/

Correspondence to - Zsolt Balogi - [email protected] and László Márk - [email protected]

Keywords - Imaging mass spectrometry, tumor marker, lipid tumor marker, S100A8, S100A9

About Oncotarget

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The cover for issue 28 of Oncotarget features Figure 5, "TMEM165 expression levels alters N-linked glycosylation," by Murali, et al.

Volume 11, Issue 26 of Oncotarget reported that Lung cancer is of particular importance, as it is the deadliest cancer worldwide.

In this study, the authors show that high mi R-708 expression is associated with survival rates in lung squamous cell carcinoma patients. mi R-708 also represses PGE2 production by suppressing both COX-2 and mPGES-1 expression in lung cancer cells.

Moreover, mi R-708 decreases proliferation, survival, and migration of lung cancer cells, which can be partially attributed to mi R-708's inhibition of PGE2 signaling.

Lastly, they identify novel mi R-708 predicted targets and possible regulators of mi R-708 expression in lung cancer.

Collectively, these data demonstrate that dysregulated mi R-708 expression contributes to exacerbated PGE2 production, leading to an enhanced pro-tumorigenic phenotype in lung cancer cells.

Dr. Carol S. Lutz from The Department of Microbiology, Biochemistry, and Molecular Genetics at Rutgers Biomedical & Health Sciences, New Jersey Medical School, School of Graduate Studies in Newark New Jersey USA said, "Lung cancer is the most common cancer, with more than 2.09 million lung cancer cases worldwide in 2018."

More importantly, lung cancer is the deadliest cancer in the world, with more than 1.79 million lung cancer-related deaths in 2018.

Lung cancer is a collection of several distinct subtypes, with non-small cell lung cancer accounting for 85% of all lung tumors. mi R-708 also indirectly regulates the expression of genes involved in PI3K signaling, cell cycle progression, epithelial-mesenchymal transition, and cancer cell stemness.

In this study, the authors aim to decipher novel mi R-708 targets and suggest a solution to the controversy on whether mi R-708 is an oncogenic or tumor-suppressive mi RNA in lung cancer.

The Lutz Research Team concluded in their Oncotarget Research Paper that collectively, their findings suggest further study of mi R-708 in lung cancer.

The data paired with previous studies highlight a potential value for mi R-708 as a diagnostic in differentiating lung tumors, as well as a potential therapeutic intervention, particularly in lung squamous cell carcinomas.

Their work has identified novel tumor-suppressive mi R-708 functions by suppressing oncogenic PGE2 production through targeting of COX-2 and mPGES-1.

These findings could be the foundation for identifying novel mi R-708 targets, as well as regulators of mi R-708 expression in cancer.

Moreover, the study highlights the need to better understand lung cancer biology to improve the diagnosis and treatment of lung cancer, ultimately aiming to increase positive patient outcomes.

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DOI - https://doi.org/10.18632/oncotarget.27614

Full text - https://www.oncotarget.com/article/27614/text/

Correspondence to - Carol S. Lutz - [email protected]

Keywords - miR-708-5p, miR-708, lung cancer, COX-2, mPGES-1

About Oncotarget

Oncotarget is a weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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Oncotarget Volume 11, Issue 27 reported that Epithelial-mesenchymal transition (EMT) and its reverse process mesenchymal-epithelial transition are central to metastatic aggressiveness and therapy resistance in solid tumors.

While molecular determinants of both processes have been extensively characterized, the heterogeneity in the response of tumor cells to EMT and MET inducers has come into focus recently and has been implicated in the failure of anti-cancer therapies.

Recent experimental studies have shown that some cells can undergo an irreversible EMT depending on the duration of exposure to EMT-inducing signals.

While the irreversibility of MET, or equivalently, resistance to EMT, has not been studied in as much detail, evidence supporting such behavior is slowly emerging.

Here, the authors identify two possible mechanisms that can underlie resistance of cells to undergo EMT: epigenetic feedback in ZEB1/GRHL2 feedback loop and stochastic partitioning of biomolecules during cell division.

Identifying the ZEB1/GRHL2 axis as a key determinant of epithelial-mesenchymal plasticity across many cancer types, the authors use mechanistic mathematical models to show how GRHL2 can be involved in both the above-mentioned processes, thus driving an irreversible MET. This study highlights how an isogenic population may contain subpopulation with varying degrees of susceptibility or resistance to EMT, and proposes a next set of questions for detailed experimental studies characterizing the irreversibility of MET/resistance to EMT.

Dr. Herbert Levine from The Center for Theoretical Biological Physics at Rice University as well as The Department of Physics at Northeastern University and Dr. Mohit Kumar Jolly from The Centre for BioSystems Science and Engineering at The Indian Institute of Science said: "Epithelial-Mesenchymal Transition (EMT) is a cell biological process involved in driving cancer metastasis and therapy resistance the two grand clinically unsolved challenges."

These hybrid E/M phenotypes may drive collective cell migration as clusters of tumor cells and can be more aggressive than cells in pure epithelial or mesenchymal phenotypes.

Recent experiments decoding the dynamics of EMT/MET using live-cell imaging and/or induction and withdrawal of various EMT-inducing external signals such as TGF? or tuning the levels of EMT-specific transcription factors have provided important insights into the reversibility of EMT and MET. Cells induced to undergo EMT for shorter durations may revert to an epithelial state after withdrawal of the signal/stimulus.

However, similar investigations about the irreversibility of MET, or in other words, the resistance of epithelial cells to undergo EMT in response to EMT-inducing signals, remain to be done.

Here, the authors' propose two independent mechanism that may explain the resistance of epithelial tumor cells to undergo EMT:

1) epigenetic feedback mediated via GRHL2?an MET-inducing transcription factor ; and

2) stochastic partitioning of parent cell biomolecules among the daughter cells at the time of cell division.

Conversely, here, the authors' show that incorporating this epigenetic feedback loop acting on the inhibition of ZEB1 by GRHL2 can cause an irreversible MET. Cells undergoing irreversible MET may exhibit resistance in undergoing EMT when exposed to EMT-inducing signals.

The Levine/Jolly Research Team concluded in their Oncotarget Research Paper that their results offer mechanistic insights into two possible mechanisms that may drive varying degrees of susceptibility and resistance to undergoing EMT in response to an EMT-inducing signal in a given isogenic population.

Full text - https://www.oncotarget.com/article/27651/text/

The cover for issue 27 of Oncotarget features Figure 4, "(A) Bimodal imaging examples of control and treated tumors (red) before and after the treatment period," by Browning, et al. and reported that the authors developed a 3-dimensional bioprinted skin model of cutaneous squamous cell carcinoma (cSCC) tumors together with a microscopy assay to test chemotherapeutic effects in tissue.

Fluorescence-derived imaging biomarkers indicated that 50% of cancer cells were killed in the tissue after 1μM 5-Fluorouracil 48-hour treatment, compared to a baseline of 12% for untreated controls.

The imaging biomarkers also showed that normal keratinocytes were less affected by treatment than the untreated tissue, which had no significant killing effect.

Data showed that 5-Fluorouracil selectively killed cSCC cells more than keratinocytes.

The authors' 3DBPS assay platform provides the cellular-level measurement of cell viability and can be adapted to achieve non-destructive high-throughput screening in bio-fabricated tissues.

Dr. Daniel S. Gareau from The Laboratory for Investigative Dermatology at The Rockefeller University, New York said, "Global incidence of cSCC is 2.2 million people and accounts for most of the ~10,000 annual non-melanoma skin cancer deaths in the United States."

Drug discovery for small molecule therapies to treat locally advanced/inoperable or metastatic cSCC and other cancers can be accelerated using patient-specific, physiologically relevant models amenable to high-throughput screening.

Models should mimic the tumor microenvironment, given its influence on tumor progression and metastasis, and should reproduce in vivo tumor cell physiochemical signaling and mechanical cues from the surrounding tissue extracellular matrix.

Animal models may not be readily translatable to human cancer treatment, and three-dimensional tissue culture models offer a viable alternative for pre-clinical screening of small molecule therapeutics.

3D models using human-derived cell lines offer increased complexity and physiological fidelity compared with two-dimensional monocultures and have been developed for several cancer models, including melanoma, pancreatic cancer, and cervical cancer.

In the disease model presented here, A431 cSCC spheroids were introduced into the tissue, and histopathology and cDNA microarray analysis was used to confirm the biological fidelity of the cancer model.

The authors' objective was to quantify the therapeutic efficacy of a standard of care treatment for a cSCC skin tissue model that recapitulates the microenvironment in which this cancer grows.

The Gareau Research Team concluded in their Oncotarget Research Paper that the model described provides a higher degree of clinical relevance because it enables the testing of chemotherapeutics against tumor cell growth in a tissue-specific context, thus capturing any potential interactions between the tumor and its microenvironment.

They envision that this model could be adopted in a “bedside” manner and applied to cells from cSCC patient tumor biopsies.

DOI - https://doi.org/10.18632/oncotarget.27570

Full text - https://www.oncotarget.com/article/27570/text/

Correspondence to - Daniel S. Gareau - [email protected].

Keywords - squamous cell carcinoma, screening, 3D printing, in vitro model, confocal microscopy

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Oncotarget Volume 11, Issue 27 published "Correction of the NSE concentration in hemolyzed serum samples improves its diagnostic accuracy in small-cell lung cancer" by Genet et al. which reported that this study aimed to develop a hemolysis correction equation and evaluate its role in small-cell lung cancer (SCLC) diagnostics.

A hemolysis correction equation was obtained by analyzing the relationship between the measured Neuron-specific enolase (NSE) concentration and the degree of hemolysis.

Correction of the measured NSE concentration in patients suspected of lung cancer caused an increase in AUC and a significantly lower cut-off value for SCLC detection when compared to uncorrected results.

Therefore, a hemolysis correction equation should be used to correct falsely elevated NSE concentrations.

Application of the equation illustrates the importance of hemolysis correction in SCLC diagnostics and questions the correctness of the currently used diagnostic cut-off value.

Dr. Daan van de Kerkhof from The Catharina Hospital Eindhoven as well as The Máxima Medical Center said, "Neuron-specific enolase (NSE) is a dimeric metalloenzyme which functions as a cell specific isoenzyme of the glycolytic enzyme enolase."

Furthermore, improved discrimination of the two main lung cancer subtypes, SCLC and non-small cell lung cancer was achieved when applying a diagnostic cut-off value of 25 ng/mL NSE or analyzing multiple protein tumor markers such as NSE and progastrin-releasing peptide at the same time.

Considering the use of NSE in lung cancer diagnostics and the medical actions that may follow, accurate and reliable quantification of NSE is of main importance.

However, previous studies evaluating the prognostic value of NSE in lung cancer diagnostics did not apply exclusion criteria or did not include the effect of hemolysis on the measured NSE concentration as such, while other factors that could influence serum tumor marker concentrations were addressed.

Therefore, this study aimed to develop, validate and apply a hemolysis correction equation that nullifies the effect of hemolysis on NSE quantification in samples of adult patients.

Using this equation, the effect of hemolysis correction on the NSE cut-off value in SCLC diagnostics was evaluated and the maximum acceptable degree of hemolysis for reliable correction was established.

The Kerkhof Research Team concluded in their Oncotarget Research Paper, "this study demonstrates that a hemolysis correction equation improves diagnostic accuracy of serum NSE concentrations in patients suspected of lung cancer. A hemolysis correction equation is therefore suggested to be incorporated in NSE-based clinical decision making, bearing in mind that results of samples with an H-index above 30 μmol/L should not be reported to clinicians."

DOI - https://doi.org/10.18632/oncotarget.27664

Full text - https://www.oncotarget.com/article/27664/text/

Correspondence to - Daan van de Kerkhof - [email protected].

Keywords - small-cell lung cancer, protein tumor markers, neuron-specific enolase, hemolysis correction equation

About Oncotarget

Oncotarget is a weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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Oncotarget Volume 11, Issue 27 published "Clonality and antigen-specific responses shape the prognostic effects of tumor-infiltrating T cells in ovarian cancer" by Tsuji et al. which reported that to delineate the complexity of anti-tumor T-cell responses, the author's utilized a computational method for de novo assembly of sequences from CDR3 regions of 369 high-grade serous ovarian cancers from TCGA, and then applied deep TCR-sequencing for analyses of paired tumor and peripheral blood specimens from an independent cohort of 99 ovarian cancer patients.

In the validation cohort, the authors' discovered that patients with low T-cell infiltration but low diversity or focused repertoires had clinical outcomes almost indistinguishable from highly-infiltrated tumors.

They also found that the degree of divergence of the peripheral repertoire from the TIL repertoire, and the presence of detectable spontaneous anti-tumor immune responses are important determinants of clinical outcome.

Also that the prognostic significance of TILs in ovarian cancer is dictated by T-cell clonality, degree of overlap with peripheral repertoire, and the presence of detectable spontaneous anti-tumor immune response in the patients.

These immunological phenotypes defined by the TCR repertoire may provide useful insights for identifying “TIL-low” ovarian cancer patients that may respond to immunotherapy.

Dr. Kunle Odunsi from The Center for Immunotherapy as well as The Department of Gynecologic Oncology at Roswell Park Comprehensive Cancer Center said, "The presence of tumor-infiltrating lymphocytes (TILs) is a key determinant of clinical outcome in a wide range of solid tumors including ovarian cancer."

High-throughput next-generation sequencing has made it possible to read the entire CDR3 to uniquely identify specific T cell clones and to estimate the absolute frequency of T cell clones in tumor tissue from the copy number of TCR sequences.

The importance of TCR repertoire in shaping anti-tumor immunity in ovarian cancer was recently demonstrated using unbiased functional analysis of TCR repertoires from TILs derived from two patients.

Tumor reactivity was revealed in 0–5% of tested TCRs indicating that the vast majority of T cells infiltrating ovarian tumors were irrelevant for tumor recognition.

To determine how the TCR repertoire of TILs shapes the prognosis of ovarian cancer patients, the authors' utilized a new computational method for de novo assembly of sequences from CDR3 regions using paired-end RNA-seq data from the Cancer Genome Atlas study of high-grade serous ovarian cancers.

The author's examined TCR repertoire in the context of the degree of tumor infiltration by T cells, spontaneous immune responses against bona fide TAAs, and clinical outcome.

The Odunsi Research Team concluded in their Oncotarget Research Paper that despite these limitations, this study highlights the extraordinary diversity of the T-cell repertoire in ovarian cancer patients, and demonstrates that pre-existing immunity against cancer antigen is a critical prerequisite to correctly understand the prognostic significance of the T-cell repertoire in the tumor and peripheral blood of patients with ovarian cancer.

They have distilled TCR repertoire information into candidate biomarkers that may critically influence the prognosis of ovarian cancer patients.

Conceptually, ovarian cancers may not fit into the classic paradigm of ?cold' and ?hot' based on the number of T cells they contain, but also by the TCR repertoire information, which serves as a surrogate for tumor recognition.

The latest technologies put these prognostic features in clinical reach not only for predicting prognosis but potentially for determining the best immunotherapeutic strategy for each patient.

Full text - https://www.oncotarget.com/article/27666/text/

Correspondence to - Kunle Odunsi - [email protected].

Keywords - T-cell repertoire, ovarian cancer, tumor immunity

Oncotarget Volume 11, Issue 27 published "Australian experience of peptide receptor radionuclide therapy in lung neuroendocrine tumours" by Lim et al. which reported peptide receptor radionuclide therapy (PRRT) is an approved treatment modality for gastroenteropancreatic neuroendocrine tumours, although Phase III randomised clinical trial data is not available for NETs of other site of origin, in practice, PRRT is used more widely in clinical practice, based on its mechanism of targeting the somatostatin receptor.

A retrospective chart review of patients with TC and AC who received 177Lu-dotatate PRRT between January 2002 and June 2019 in six hospitals across Australia was undertaken.

Forty-eight patients received a median of four 177Lu-dotatate treatments.

The response rate to 177Lu-dotatate was 33%, with a median overall survival of 49 months, at a median follow up of 33 months.

177Lu-dotatate PRRT in patients with lung NETs is used in real world practice, where it appears well-tolerated with some efficacy.

Dr. Lisi Elizabeth Lim from The Department of Medical Oncology at Monash Health said "Neuroendocrine tumours (NETs) are uncommon malignancies, comprising 0.5% of all cancers."

Lung is the primary site for approximately 20?25% of NETs; conversely NETs comprises about 2% of all lung malignancies.

New trials have demonstrated that adequate numbers of patients can be recruited through global collaborations, both for protocols specific to lung NETs and those recruiting patients with NETs from a variety of sites.

PRRT is a firmly established treatment modality for advanced GEP NETs following the publication of the landmark NETTER-1 trial, where patients with progressive midgut NET were randomised to receive 177Lu-dotatate with ongoing octreotide long-acting repeatable therapy, or high dose octreotide LAR alone.

The significant benefit for PRRT in midgut NETs has provoked debate about whether randomised trials are required to prove its efficacy in NETs of other site of origin.

NET consensus guidelines either omit specific comment on the use of PRRT in lung NETs, or state that imaging with SSTR-PET can assist in identifying patients who may benefit from PRRT. The Lim Research Team concluded in their Oncotarget Research Paper that further data will be forthcoming also from studies of PRRT in patients with SSTR-expressing tumours of histologies other than NET. The randomised phase II LUTHREE trial is inclusive of all SSTR positive tumour types, and is not restricted to NETs. The POLNETS trial is also extending the use of PRRT to paraganglioma and pheochromocytoma, in addition to advanced NETs of any site of origin.

DOI - https://doi.org/10.18632/oncotarget.27659

Full text - https://www.oncotarget.com/article/27659/text/

Correspondence to - Lisi Elizabeth Lim - [email protected].

Keywords - lung, carcinoid, atypical, neuroendocrine, peptide receptor radionuclide therapy

About Oncotarget

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Volume 11, Issue 26 of Oncotarget reported that in this study the authors studied the differences in mi RNA expression between sporadic and FAP-associated Desmoid tumors using microarray confirmed by quantitative PCR.

Among them, mi R-133b levels were significantly lower in FAP-associated Desmoid tumors than in sporadic Desmoid tumors. The qPCR analysis showed that SIRT1 mRNA levels were significantly up-regulated in FAP-associated Desmoid tumor than in sporadic Desmoid tumor, whereas no differences in ELAVL1 expression was observed between these two Desmoid tumor types.

In addition, a negative correlation was observed between mi R-133b and SIRT1 in FAP-associated Desmoid tumors, but not in sporadic Desmoid tumors The mi R-133b-SIRT1-β-catenin axis may represent a novel mechanism underlying progression of FAP-associated Desmoid tumor.

Dr. Maria Teresa Rotelli from The Department of Emergency and Organ Transplantation at The University of Bari “Aldo Moro” in Bari Italy said, "Desmoid tumor (DT) is a rare, mesenchymal benign tumor, characterized by monoclonal, fibroblastic proliferation with local invasiveness, high risk of recurrence and even mortality, despite metastatization never occurs."

The CNNTB1 mutations have been found in approximately 85% of DTs by routine Sanger sequencing, however, using a highly sensitive technique like next-generation sequencing, they may account for 90–95% of sporadic DT cases.

In these DTs, the germline mutations in the APC gene are responsible for the nuclear accumulation of β-catenin.

While the risk of death in sporadic DT is low, FAP-associated DTs are the most frequent cause of death in patients with FAP after the colon has prophylactically been removed.

It must be emphasized that the disruption of the Wnt signaling represents a common pathway in both DT forms, but sporadic and FAP-associated DTs are associated with mutually exclusive molecular alterations.

In a previous study, the authors have investigated a possible correlation between mi RNA expression and CTNNB1 mutations in sporadic DTs.

The Rotelli Research Team concluded in their Oncotarget Research Paper that the dialog between MSCs and tumor cells in FAP-associated DT tissue microenvironment could lead to β-catenin deacetylation driven by SIRT1, promoting Wnt/β-catenin signaling cascade in this tumor.

Although the number of specimens of FAP-associated DTs used in the present study was limited, it could be speculated that the β-catenin deacetylation process in FAP-associated DTs mimics the stabilization of that protein induced by CTNNB1 gene mutations occurring in sporadic DTs.

Therefore, in addition to APC gene mutations, the mi R-133b-SIRT1-β-catenin axis may represent a novel mechanism underlying the progression of FAP-associated DT. However, further studies are needed to fully understand the influence of mi R-133b-SIRT1 in the genesis or progression of FAP-associated DT.

DOI - https://doi.org/10.18632/oncotarget.27622

Full text - https://www.oncotarget.com/article/27622/text/

Correspondence to - Maria Teresa Rotelli - [email protected]

Keywords - desmoid tumor, miRNA, familial adenomatous polyposis, B-catenin, Wnt pathway

About Oncotarget

Oncotarget is a weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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